Thursday, July 12, 2012

Interview with Aitor Calero of Directo al Paladar

Aitor Calero writes for the popular Spanish cooking and nutrition blog, Directo al Paladar ("straight to the palate"). We did a written interview a while back, and he agreed to let me post the English version on my blog. The Spanish version is here and here.

Without further ado, here it is:

Whole Health Source, why did you choose that name for
your blog and why did you decide to start a blog?

I began writing about seven years
ago because I felt I had useful information to share. Whole Health Source was actually the name of
my original website. It was intended to
be a nutrition and health site, but due to my poor web development skills, it
was very amateur looking! I took it down
shortly after starting my blog because I felt the information was
outdated. I chose the name Whole Health
Source because it implies that health is more than just not having a disease,
and that many factors converge to determine health.

What is the "state of the art" in nutrition
science, what theories are right now more advanced?

I’m fairly specialized in my
research so I’m perhaps not the best person to say what’s state of the art in
the field as a whole, but I’ll give my perspective on a few things that I find
compelling.

One of the things that I’ve found
really gratifying is seeing the field move in the direction of studying foods
rather than specific nutrients.
Essential nutrients such as minerals and vitamins are obviously
important, but now that we really understand the great biological complexity of
whole foods, it’s becoming less and less plausible that we can accurately
predict the biological impact of a food by understanding only a few of its
chemical components. A number of
prominent researchers understand this and are moving their research in that
direction.

Another line of investigation that’s
important is understanding how genes and environment interact to produce health
or disease—this field will continue expanding and providing important
insights. There is no one-size-fits-all
solution for health.

Gut bacteria and digestive health
have also generated a lot of interest lately.

There is a lot of cutting-edge
research going into understanding the brain mechanisms that mediate food
intake. We’re getting to the point where
we can predict obesity risk to some degree just by measuring cognitive traits
(e.g., ability to delay gratification, impulsiveness, susceptibility to
reward), or brain responses to food stimuli.
Also, understanding how the energy homeostasis system in the brain is
altered during the development of obesity—this is my field.

What is the real role of physical activity? Some argue
that the more you exercise the more hunger, is that correct?

I think a person would have to be
pretty stubborn at this point to think that physical activity doesn’t help at
all with body weight control and general health, given the state of the
evidence. For obesity, it seems to work
best as a preventive measure rather than as a treatment, and this has been
strongly supported both by animal studies and observational studies in
humans. It’s hard to return to true leanness
once a person is obese, no matter what strategy they use. As we say, “an ounce of prevention is worth a
pound of cure”. It is correct in a
general sense that exercise increases hunger.
However, on average it doesn’t increase hunger enough to make up for the
calories you expended, and therefore you lose fat if you’re overweight.

There is a lot of individual
variability here. Research has shown
that some overweight people compensate for exercise by eating more, and others
don’t, and in some cases they even eat less than if they hadn’t exercised. On average, exercise alone isn’t a very effective
way to lose fat if you have a lot to lose, but it can increase the
effectiveness of dietary interventions.
However, some people respond exceptionally well to exercise and can lose
20, 30, 50 pounds. Regardless of whether
or not it can turn people from fat to ripped, regular exercise is an absolutely
essential component of a healthy lifestyle.

You have debated with Gary Taubes about the role of
insulin and carbs in weight control, what is right or wrong with his view?

I think Taubes has been useful in
the sense that he introduced many people to the low-carbohydrate diet, and the
research challenging some of our conventional ideas about the health impacts of
such diets. A number of studies on
low-carbohydrate diets have shown that although they’re higher in fat and meat
than most diets, when adopted by overweight or obese people they’re able to
safely cause fat loss and health improvements over periods lasting up to two
years. No one really knows what happens
after that. They seem to cause more fat
loss, and perhaps better metabolic improvements, than the conventional low-fat
diet for periods up to one year.
Although the ability of low-carbohydrate diets (and most diets in
general) to cause fat loss is fairly modest in most clinical trials, some
individuals respond extremely well to it and can lose large amounts of
fat. For these people, the diet can be
life-changing.

However, Taubes took this piece of
useful information and stretched it much too far. He ditched most of the last 70 years of
published research and constructed a mechanism whereby many of our modern
health ills, particularly obesity and diabetes, are due to the ability of
carbohydrates (particularly refined carbohydrate and sugar) to increase
circulating insulin. It’s an extremely
simple model if you think about it: carbs -> insulin acting directly on fat
cells -> obesity. Much too simple in
fact, given the many roles of insulin in various tissues including the brain,
not to mention all the other processes that occur with food ingestion. Taubes has scathingly criticized seasoned
researchers for not considering his hypothesis, which he felt was correct but ignored
by researchers for non-scientific reasons (do I need to point out here that
Taubes has virtually no training or experience in the biological sciences?). The reality is that researchers have not
overlooked the hypothesis, they have tested it in many different ways and found
that it does not explain obesity. As a
scientist, I can’t say with 100 percent confidence that elevated insulin plays
no role in obesity whatsoever, but what I can say with 99.99 percent confidence
is that no single factor will ever be able to explain common obesity. I can also say with confidence that there are
much more compelling explanations than excess insulin acting on fat cells, and
these are currently being pursued by many brilliant researchers.

Is fructose a problem as Dr. Robert Lustig suggests?

Humans have a very long evolutionary
history with fruit. Our ancestors were
among the first organisms to eat fruit 55 million years ago, shortly after it
evolved. Mammals likely evolved into primates
specifically to access fruit, and our ancestors remained in trees eating fruit until
relatively recently. Our closest living
relatives the chimpanzees get most of their calories from fruit, and they
therefore have a high-sugar diet. All
human cultures that have access to fruit enjoy it and eat it regularly.

Studies suggest that fruit is
healthy and can even aid fat loss a little bit under certain circumstances. However, most of the sugar people eat doesn’t
come from fruit—it comes from processed corn or refined sugar cane juice. This poses a problem for several
reasons. The first is that sugar and
high-fructose corn syrup are virtually devoid of micronutrients and other
beneficial substances, therefore they crowd out more nutritious food. The second is that sugar increases the energy
density and palatability of foods, leading to increased meal size and
eating/drinking between meals in the absence of hunger/thirst. This contributes to obesity and all the
things that come along with it.

The third problem is that yes, in
excess refined sugar can cause metabolic problems, and this is mostly due to
its fructose content. To my knowledge,
this has only ever been demonstrated with large amounts of refined sugar or
fructose, and never with fruit. Lean
people are more resistant to the insulin resistance and other metabolic
problems that occur with fructose feeding, and this probably relates to the
energy overload already present on the liver in obesity. It’s not clear whether or not the amount of
fructose most people eat today is enough to cause these problems, however I
suspect that for people eating more sugar than average, it is. Despite its ability to cause metabolic
problems in excess, many studies have shown that fructose is no more fattening
than other equally caloric sweet substances (such as glucose).

Is insulin the main problem? What about ghrelin,
leptin and other hormones?

Insulin resistance (an inability of
insulin to do its job properly) is definitely a central problem for health in
the 21st century. It
contributes to many different health conditions, particularly type II
diabetes. The main cause of insulin
resistance is excess body fat, plain and simple, although there are many other
factors such as exercise and diet quality that also have an impact. To understand insulin resistance, we have to
understand what causes excess body fat.
Food intake is regulated by a “symphony” of signals that the brain
receives and uses to determine whether or not a person will eat. Some of these signals are from sensory organs
and the brain itself, while others are hormones in the circulation coming from
the gut, body fat, the pancreas, and elsewhere.
This finely tuned system is disrupted when a susceptible person is
exposed to abundant, energy-dense, tasty food, in an environment that minimizes
physical activity and sleep, and promotes psychological stress. Leptin is a key hormone that restrains food
intake in this context, but it can only go so far. Eventually, leptin resistance develops, which
makes it difficult to lose fat once obesity is established.

Is wheat that bad? If so, why?

Wheat is definitely bad for about
one percent of Europeans and Americans who have celiac disease. This alone is a major public health burden
attributable mostly to wheat. Beyond
that one percent, I suspect that there are many other people who benefit from
avoiding it for various reasons, but that is a supposition that will require
more research to confirm. There are
probably many people who can eat wheat with impunity.

I think one of the most problematic
aspects of wheat is that it’s used to make things that are energy-dense and
taste really good. Flour is a substance
that can be homogenously mixed with fats, sugars, and flavorings, creating
combinations that are virtually irresistible to the palate. Think brownies, cookies, cake, and even a hot
loaf of crusty bread. Most people can
find room for 200 calories of chocolate cake even when they’re stuffed at the
end of a meal. Can you get that excited about
a plain potato?

A fellow named Matt Lentzner
organized something called “Gluten-Free January” last year where people gave up
gluten for one month. An epidemiologist named
Dr. Janine Jagger and I composed surveys to collect anonymous information from
participants at the end of the month. We
found that almost everyone who was overweight lost several pounds, and almost
everyone with digestive problems and low energy noticed an improvement (1, 2). There was no control group so we don’t know
how much of the improvement was due to avoiding gluten per se, how much was due to avoiding junk food and/or reducing
carbohydrate, and how much was a placebo effect. However, it does suggest that many people
benefit from giving up gluten, whatever the mechanism may be.

What about fats? Why they have been so criticized? What
are the real dangerous fats?

Fats are energy dense, and saturated
fats can increase circulating cholesterol in controlled trials, therefore it
was thought that fats contribute to obesity and coronary heart disease. I think it’s still true that fat can
contribute to obesity if it increases the energy density and palatability of
food. However, paradoxically dietary fat
is compatible with body fat loss in the context of a low-carbohydrate diet, so
it’s not a simple relationship. The key in
that context is that something is being restricted. High fat in combination with high
carbohydrate will not cause fat loss.

Saturated fat has received a lot of
blame over the years, but it’s becoming increasingly likely that it plays
little or no role in heart disease in humans, in the context of a normal
diverse diet. That doesn’t mean a person
should put a huge amount of butter on everything or drink coconut oil, but in
moderation as part of a mixed whole food diet, I don’t see any reason to be
concerned about eating the natural fats contained in meat, dairy, eggs, and
nuts, and to a lesser extent using fats like butter, unrefined coconut oil, red
palm oil, and extra virgin olive oil in cooking.

I’m not a proponent of refined seed
oils (“vegetable oils”). They’re refined
and therefore contain virtually no nutritional value, and many of them (e.g.
cottonseed and soy) are by-products of other industries. Furthermore, they tend to be high in
polyunsaturated fat and are therefore susceptible to oxidation (rancidity)
during cooking, and most of them contain a lot of omega-6 and very little
omega-3, which can potentially disrupt many processes in the body (there are
exceptions, such as canola oil). If you
must use a refined seed oil for cooking, the best is probably high-oleic
sunflower oil, a variety bred for low polyunsaturated and high monounsaturated
fat content.

Do we have to be worried about cholesterol? Can we
control it through diet or drugs?

Cholesterol in the blood is
contained in particles called lipoproteins.
Lipoproteins such as LDL (“bad” cholesterol) and HDL (“good”
cholesterol) are causally related to the development of atherosclerosis
(thickening and degeneration of the arteries), which increases heart attack
risk. So yes, I think we should be worried
about cholesterol. The ratio of total
cholesterol to HDL cholesterol is a simple and effective indicator of risk. For people who are interested, the Framingham
risk calculator can give an estimate of 10-year heart attack risk based on data
collected from the Framingham study (3).

Diet and drugs do have an impact on
lipoproteins. Excess body fat increases
LDL and decreases HDL, and fat loss can reverse this to some extent. Polyunsaturated fat lowers LDL and HDL. Saturated fat increases LDL and HDL in trials
lasting up to three months, although it’s not clear to what degree this effect
persists in the long term (in any case, it appears to have little or no impact
on heart attack risk). Dietary
cholesterol has a modest ability to increase LDL and HDL. Moderate alcohol consumption and exercise
increase HDL and reduce heart attack risk.
Smoking cigarettes lowers HDL and greatly increases heart attack risk,
while smokeless tobacco does not.

Drugs such as statins lower LDL and
reduce heart attack risk. These drugs do
have side effects for some people, but they’re probably worth it in high-risk
individuals.

Your main point is that the reward and palatability
plays a huge role in hunger and appetite? Why?

Food reward is the seductiveness of
food—its ability to motivate you to seek it out and eat it. Palatability is a related concept—it’s the
pleasure derived from eating a food.
It’s really just common sense that if a food is seductive and tastes
really good, you’re going to eat more of it, and you may even eat it between
meals when you aren’t hungry.

Our
ancestors lived in a world of simple foods.
Even just a few hundred years ago, they didn’t have modern stoves, they
didn’t have a spice rack, they often didn’t have cooking oils, sweeteners, or
salt. They certainly didn’t have soda,
candy bars, and French fries. They ate
simply prepared whole foods, and this allowed their appetite control mechanisms
to operate correctly, effortlessly matching energy intake to energy needs.

I won’t get into the details of the
mechanism, but if food is highly rewarding and palatable, it modifies these
appetite control mechanisms, allowing you to eat more and accumulate more body
fat than you would if the food were more simple. In the US and globally we are increasingly
surrounded by energy-dense, highly rewarding and palatable foods, and food cues
in advertising that make us crave them.
We eat less home-cooked food than ever before, instead outsourcing our
food preparation to professionals who attempt to get our business by maximizing
reward and palatability.

In Europe, the Dukan Diet is gaining traction as a way
to lose weight, do you know it? What do you think?

The induction phase of the Dukan
diet is basically a modified version of a protein-sparing modified fast
(PSMF). PSMF diets have been around for
a long time—they’re basically very high protein low-calorie diets that cause
rapid fat loss while minimizing hunger and muscle loss due to the blandness,
reduced carbohydrate, and high protein content.
PSMF combines a low-fat and a low-carbohydrate diet. PSMF diets contain very little carbohydrate
or fat, and in Dukan’s case they are also quite bland. This all contributes to the appetite suppressing
effect of the diet, facilitating fat loss.
It also resets the palate to some degree, diminishing psychological
reliance on highly rewarding/palatable foods.

That’s OK for a while as long as you
can tolerate the high protein and low calories, but obviously the diet is not
nourishing enough to be a long-term solution, so it must give way to a
maintenance phase. This is where things
become difficult, because most people will rapidly regain lost fat. However, if you’re prepared to make positive
and lasting changes to your diet and lifestyle, and never return to how you
were living before, then it’s possible that you could maintain some or even
most of the fat loss.

Stephan, This is a great summary of a lot of nutritional issues. You do a good job on controversial areas in which some people go overboard about one nutrient or the other.

I've found that it's sometimes necessary to overstate a point in order to get people's attention.

So I don't get upset if someone comes up with a new extreme diet. It may work for some folks but not for others.

However, I disagree with two of your points:

1. That insulin resistance is caused by excess weight, period. About 50% of IR is genetic, and different ethnic groups have different levels of IR even when slim.

2."Even just a few hundred years ago, they didn’t have modern stoves, they didn’t have a spice rack, they often didn’t have cooking oils, sweeteners, or salt."

Maybe they didn't have a spice rack, but they had spices. They had sugar, and if they didn't, they used sweeteners like honey or made maple syrup. They had salt, although it could be expensive in some parts of the world and people would go to great effort to get it.

I have a 15th century cookbook, and the recipes call for a lot of spices. Ginger and sugar are mentioned frequently, as well as cloves and mace.

A recipe for roasted partridge ends with "And kutte him so; or elles ete him with sugar and mustard."

This book "A Fifteenth Century Cookry Boke" or similar ones are probably still available and might help to understand what people (at least rich people) were eating then.

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I just wanted to add that the Dukan Diet also includes large amounts of soluble fiber in the form of oat bran. I live in France and the supermarket shelves are full of Dukan bars, biscuits and breakfast cereals. All of them are based in oat bran with some kind of protein isolate added in so it will fulfill the prescription of a PSMF.

We have a "cousine" here who lost a lot of weight initially on the diet, then just as I predicted, gained it all back by the time we saw her next. I feel like if Dukan had allowed her more room to eat fiber in the form of fruits and vegetables, she would have not felt deprived and kept the weight off. She herself admits now that the diet was "too hard to stay on". Especially in France, I would add. Not an easy place to refuse food!

Sorry, my point about the soluble fiber was that it fills you up, rids your body of excess estrogen and compensates for the high protein you're getting with the Dukan diet. It may also have effects on your brain and setpoint, since all of it is hitting the nerve terminals in the ileum when you eat. Unlike fat.

This helps the dieter fill up on what, only eating protein and no fat, would actually be a very small volume of food. And anyone who's ever dove into a bowl of oat bran for breakfast knows it's about the most boring thing you can eat (especially if you're not allowed to put sugar on it -yuck).

The main cause of insulin resistance is excess body fat? What about loss of pulsatile insulin secretion? According to Steve O'Rahilly, insulin target tissues require periodic absence of insulin to maintain their sensitivity. I don't think your series on insulin resistance mentioned this.

The chronic low-grade inflammation that accompanies obesity was recently shown to disrupt calcium oscillations in beta cells on which insulin oscillations depend.http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2948622/

This suggests it isn't the excess body fat per se that causes insulin resistance, it's the inflammation. Perhaps this is what you meant. However, if the excess body fat is due to eating palatable food, there's a problem. How does palatable food cause inflammation?

Agree with point 2 from Gretchen on the kinds of spices eaten hundreds of years ago. I recommend reading "Out of the East: Spices and the Medieval Imagination", by Yale university professor Paul Freedman. In my opinion, he puts to rest the myth that spices were used to make rotten inedible foods palatable. Instead, Freedman argued that spices were used more abundantly than they are used today in Europe; at least in wealthy homes. Cook books and recipes are some of the evidence we have left from this time period.

Having said that, I suspect that in medieval Europe obesity coincided with wealth; quite the opposite of what we're seeing today. If that is true, then I don't think the availability of spices necessarily poses a hole to your argument.

Many educated people I have spoken with feel you are going to leave your mark on obesity research. You're a very young guy still, with plenty of time to do so.

I hope the general public can see through the information on yuor blog how badly they have been conned by the "Internet fat loss experts."

Healthful, nutrient dense eating and good exercise will still be a priority for health maintenance, but:

I really hope science will actually develop an effective long term treatment for sustained weight loss, which we currently do not have . Although I cannot say how far off on the horizon it is, my guess is that in 10 to 20 years it might be here. Namely, unprecedented drugs which directly target fat cell regulation and will destroy the dogmatic failure of the last 60 years ( e.g. the caloric hypothesis dogma).

Think how much more we know now compared to even 1994.We will continue to learn with your own research, Dr. Friedman's lab, and other great scientists. It is a collaborative effort. I am fairly sure that Dr. Leibel was on Dr. Friedman's team in 1994 , but this is not mentioned by the media.

If these drugs which directly target fat cell regulation are very effective, then people such as Manuel Urbe will have genuine hope and even have their weight normalized.

Of course, the first generation will all be genuine pigs and all drugs carry some risk.

It is true that genetics has a strong influence on insulin sensitivity. Perhaps a better way of conveying what I mean is that gains in body fat over time are the main factor responsible for increases in insulin resistance and type II diabetes incidence over time. In other words, it's the main modifiable risk factor.

I think you have to be really careful drawing conclusions about the typical diet from cookbooks, particularly from as long ago as the 15th C. Only the wealthy would have produced, owned and used cookbooks, and most people probably couldn't even read them because they were illiterate.

It's true that certain spices and sweeteners were available, but they were often expensive and quantity/variety was limited. Today the average person can go to the grocery store and buy 30 different herbs and spices, 10 different sweeteners, and 10 different added fats. Virtually no one had this kind of access in the 15th C.

Most people in Europe during this time would have gotten most of their calories from one or two grains, prepared simply as porridges and/or breads. There were vegetables and fruit, but again much less variety than today, partially due to seasonality and partially because many plants hadn't been introduced yet. If they were lucky, they would supplement with dairy and/or meat for some meals. They probably used a few herbs pretty regularly from the garden, but the average person was not using pepper and nutmeg imported from Asia-- there's no way they could afford it on a regular basis.

I also think you should be very cautious about drawing conclusions from paintings. At the time, fatness was equated with health. If the painter wanted to portray an image of abundance and health, it would make sense to portray overweight people even if most people were not overweight at the time.

He sounds for me like one of many who have tendency to simplify , but who am I to judge? Some people payed attention already on his eyebrows rising statement about obesity causing IR, (rally? what about thin ones with IR and D2?) On the subject of fruits, it is often gets overlooked that fruits are seasonal in basically any environment, and many animals use it to fatten up before lean times. Here is some research that some people may find interesting.http://www.eurekalert.org/pub_releases/2011-12/dc-soo120811.php

"The Borneo environment is stressful. The soil is not very fertile and plants crop unpredictably, only producing quantities of fruit every four or five years. When they do bear fruit, the whole forest produces at once. The animals gorge themselves, put on fat, and then live off these reserves for the next three to four years. "

There are people who develop T2DM while they're lean, but it's rare. More common is that people lose weight after developing diabetes because they're sick. BMI is extremely strongly related to diabetes risk.

For example, people with a BMI of 35 or greater have a 42 times higher risk of developing T2 diabetes than people with a BMI of less than 23. Yes, you read that correctly: 42 times. Risk increases at all levels of BMI, for example even going up to 24.0-24.9 BMI increases risk by 50%. That's not even considered overweight.

www.ncbi.nlm.nih.gov/pubmed/7988316

And that's using a crude measure of body fatness, BMI. The relationship between body fatness and diabetes risk factors is much tighter when you actually measure body fat than when you estimate it with BMI.

There is absolutely no doubt that body fatness is a major risk factor for diabetes, and this should not be raising anyone's eyebrows because it has been clear for a long time. The study I cited is from 1994 and it has been corroborated by many others.

By the way, the main risk factor is not so much total body fatness itself, but ectopic fat (visceral, hepatic, intramuscular, etc). However, ectopic fat tends to increase along with total fat in most people.

Sure, Diabetes 2 is very strongly associated with an abnormal amount of body fat, for example, 80% of children with D2 in Japan are obese, but on another side, obesity din't cause diabetes in 20% of children, it was for another reason or reasons. Also, not everybody with an obesity develops D2. Of course, some people could carry just the right amount of the wrong kind of fat, as you mentioned. We all know some thin people with D2, they mostly have a family history of adult-onset diabetes (sorry, just a personal observation, can't give a link). It looks like genetic plays a big role as well.

I'm curious what your latest thinking is vis a vis blood lipids and CHD. Do you still subscribe to some variant of the "oxidized/degenerated LDL" theory, as described in posts of yours from several years ago, or articulated by Chris Masterjohn, or do you think that LDL levels in the blood, per se, influence CHD risk?

Also, in your interview, you express some caution about added oils such as butter, coconut oil, red palm, and so on- do you feel their effect on blood lipids, at least when eaten in large-ish quantities, is problematic? Is this part of why you have become increasingly supportive of a higher-carb (or at least starchy tuber;)) diet?

I'm not trying to start a debate or anything, I'm really just interested in what you have to say along these lines...

Gretchen, you're absolutely right that they're not fat-phobic, and it's no coincidence that a high-animal protein proponent like Dr. Dukan comes from France.

But there is a growing weight problem here. I would say this has more to do with eating less fresh, whole foods over the last 15 years than any trend towards eating more or less of any one macro group.

'..high fat in combination with high carbohydrate will not cause fat loss..'

I think this depends on the starting point. A wholefood diet high in fat and carbs can in theory do this, if the starting point is crap mitochondria and the wholefood diet repairs them.

I think the mistake made by Mediterranean diet advocates is to think you have to eat low-fat dairy. This can mean deficiencies of fat-soluble vitamins.

I also think it's a mistake to think fat loss should be fast. Fast fat loss means the surrounding connective tissue doesn't have time to remodel itself, so either fat breakdown stops and reverses, or you end up with loose folds of skin requiring surgery.

Jon Gabriel appears to have lost over 200 pounds without dieting, and has no loose skin at all.

Stephan, I agree that body fat can cause insulin resistance and is a strong risk factor for type 2 diabetes, although some very fat people are very insulin sensitive. What I was saying was that this IR is superimposed on genetic IR.

I also agree that then, as now, the diet of the rich was different from the diet of the poor and average. The daily diet was different from the diet on feast days. For that reason, when making generalizations like "there was no salt," it's important to specify which group you are talking about.

And re salt, according to Colin Clair's history of eating, although peasants seldom ate meat, "even the humblest house had its larder where the bacon was kept after it had been salted down for the winter months." That suggests they had access to salt and occasional access to pigs, probably wild.

I wasn't suggesting that the average person used cookbooks, but that herbs and spices were available. Some herbs like thyme grow wild and households had herb gardens. More exotic spices like cloves were the incentive for the lucrative spice trade. People risked their lives to find better routes to get the exotic spices, which implies a huge demand.

Clair says they thought fruit was unhealthy, and the kitchen gardens grew mostly herbs, with few veggies except onions and leeks.

Do we have to be worried about cholesterol? Can we control it through diet or drugs?

Cholesterol in the blood is contained in particles called lipoproteins. Lipoproteins such as LDL (“bad” cholesterol) and HDL (“good” cholesterol) are causally related to the development of atherosclerosis (thickening and degeneration of the arteries), which increases heart attack risk. So yes, I think we should be worried about cholesterol. The ratio of total cholesterol to HDL cholesterol is a simple and effective indicator of risk. For people who are interested, the Framingham risk calculator can give an estimate of 10-year heart attack risk based on data collected from the Framingham study (3). _________________________________

I think that one should not be intertwining the word cholesterol with lipoproteins as they relate to cardiovascular risk. I would suggest readers as well as each of you review the cholesterol series blogged by Peter Attia - very enlightening.

I've been following Dr. Attia's series. It is certainly true that there can be discordance between cholesterol and lipoproteins. That is why just measuring circulating cholesterol is a blunt tool. That being said, blunt tools can still be useful, as this one is.

Regardless of what's happening at the lipoprotein level, the TC:HDL ratio provides reasonable cardiovascular risk estimate on average, and this has been confirmed many times.

I thought Dr. Attia's series was really nice until he began writing about the dietary influences on lipoproteins (like fructose), at which point his critical thinking seemed to lapse.

Just because drinking 25% of calories as refined fructose causes potentially problematic lipoprotein changes, does not mean eating a mixed diet with fruit (or even a non-extreme amount of added sugar) has such an effect, and in fact the research suggests it doesn't.

If you want to create experimental atherosclerosis in animals, there are much more effective ways to do it than sugar, although it's possible that refined sugar could exacerbate the problem.

This study showed that a high fruit weight loss diet (14% energy from fructose-- this is a LOT of fruit) did not increase triglycerides, lower HDL, increase insulin resistance, or cause any other telltale negative lipid signs relative to a low-fruit diet. It also had no effect on energy expenditure relative to the low-fruit diet.

www.ncbi.nlm.nih.gov/pubmed/16395633

Another study (comparing a sucrose intake of 121 vs 12 g/day) found a similar result using refined sugar:

"Results showed that a high sucrose content in a hypoenergetic,low-fat diet did not adversely affect weight loss, metabolism,plasma lipids, or emotional affect."

www.ncbi.nlm.nih.gov/pubmed/9094871

Energy intake seems to trump sugar intake every time where metabolism and blood lipids are concerned-- although in a hypercaloric context, refined sugar probably is worse than refined starch.

To be fair, most people today live in a hypercaloric context. The point is that the root problem is excess calorie consumption, without which eating unrefined sugars in moderation is likely beneficial rather than harmful.

Good interview. Some excellent analysis, some emphasis I'd dispute, but a lot of good sense all in one place.Thanks.

Here is an interesting post on the carbohydrate-denovolipogensis-only hypercaloric? question which resolved me once again never to take anything in abstracts for granted.http://www.lucastafur.com/search/label/de%20novo%20lipogenesis

@Stephan: "There is absolutely no doubt that body fatness is a major risk factor for diabetes..."

"Risk factor" or "relationship" are just other ways of saying "correlation" and as we all know "correlation does not show causation" ...we DO all remember that... right?

Yes you can quote statistics showing that 80% of Type 2 Diabetics were overweight or obese AT THE TIME OF DIAGNOSIS but are we really so naive as to assume that the day before diagnosis they did NOT have Type 2? Or to dismiss any consideration (as just one other possible interpretation) that the same underlying metabolic disorder which ultimately leads to the Type 2 could also be responsible for the excess fat storage?

The fact that you as an accredited scientist -- required by the scientific method to rigorously consider ALL possible alternative interpretations of the observations -- that fact that you continue to spread the assumption that obesity CAUSES Type 2 is intellectually dishonest.

My comment regarding cholesterol was more related to the fact that what you posted could imply that we need to watch our cholesterol intake. Yet there is a purported lack of association of dietary cholesterol to circulating blood cholesterol.

Supposedly, the world's former heaviest man, Manuel Uribe, who once weighed 1,234 pounds ( small Japanese cars come in lighter than that) had/has no high blood pressure, no high cholesterol, no diabetes. Supposedly.

I believe something like 80 % of people who have type II diabetes are over fat or obese.

I have heard and read , (as Stephan pointed out), that weight loss can help. Only losing a good 10 pounds can cause disproportionate health benefits. The normilization of one's body weight is not necessarily needed to have tremedous health benefits from only losing 15 pounds.

I think Manuel is an exception. If it is true then it surprises the hell out of me. LOL !

But, yes about the remaining 20 % ( who are normal weight to thin) have type II diabetes.

In general, the more fat you gain the worse the outcome for increasing yuor type II diabtetes risk, especially if your lifestyle is bad as well.

People like Stephan, Dr. Michael Rosenbaum and Dr. Douglas Coleman are more qualified to speak about this though. I am not that well versed on this particular subject, or at least not in great detail.

Most of the genes associated with type 2 affect insulin secretion, not insulin resistance. Yes, higher weight in general means higher insulin resistance. But people without "diabetes genes" just secrete more insulin to compensate.

So is type 2 caused by IR or wimpy beta cells? Probably both. And ethnic groups with a lot of genetic IR can become diabetic by putting on only 10 pounds.

There may also be factors we haven't discovered yet. Some people blame toxins.

@FrankGYou made a valid point. Is the same underlying metabolic disorder which ultimately leads to Type 2 diabetes also responsible for the excess fat storage?

The answer, from some work published earlier this year, appears to be yes. The disorder is failure of autophagy.

'.. Autophagy is a catabolic cellular process involving the degradation of the cell's own components. ...the importance of autophagy in hypothalamic proopiomelanocortin (POMC) neurons, key regulators of energy balance, has not been addressed. The role of autophagy in leptin sensitivity that is critical for the control of body weight and appetite has also not been investigated. We produced mice with specific deletion of autophagy-related 7 (Atg7), an essential autophagy gene, in hypothalamic POMC neurons...[these] mice had increased body weight due to increased food intake and decreased energy expenditure. ...Our findings indicate a critical role for autophagy of POMC neurons in the control of energy homeostasis and leptin signaling. ...We and others have reported that autophagy is important in the maintenance of pancreatic β-cell mass, structure, and function...'http://www.ncbi.nlm.nih.gov/pubmed/22334718

There will always be variability in any biological phenomenon, particularly if it's multi-factorial, so it is not a surprise that obesity and insulin resistance do not have a 1:1 correspondence. Roughly 20% of obese people are resistant to the metabolic effects of excess body fat. The same is true in animals-- genetic background determines to what degree excess body fat causes insulin resistance.

Total body fat is highly (inversely) correlated with insulin sensitivity, however it may be because the fatter you get, the more ectopic fat you accumulate in your visceral depots, liver, muscle, etc. Total body fatness is well correlated with fat in these ectopic depots. Although even ectopic fat accumulation may be a marker of tissue energy overload that is not actually itself causal.

About Me

I'm a writer and science consultant with a background in neuroscience and obesity research. I have a BS in biochemistry and a PhD in neurobiology. I'm the author of "The Hungry Brain: Outsmarting the Instincts That Make Us Overeat".

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